Comprehensive Analysis of mRNA Methylation Reveals Enrichment in 3' UTRs and Near Stop Codons
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA141085 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR494613.fastq.gz | Fastqsanger.gz | |||
| SRR494614.fastq.gz | Fastqsanger.gz | |||
| SRR494615.fastq.gz | Fastqsanger.gz | |||
| SRR494616.fastq.gz | Fastqsanger.gz | |||
| SRR494617.fastq.gz | Fastqsanger.gz |
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Project description:Here, we use a novel technique for locating regions of N6-adenosine methylation (m6A) throughout the transcriptome and present a profile of m6A sites in the mouse brain. Our use of methylated RNA immunoprecipitation combined with RNA-seq (MeRIP-Seq) identifies thousands of RNAs which contain m6A sites. In addition, we find that regions of m6A formation are particularly enriched near stop codons, which might provide clues into the potential funciton of this highly prevalent RNA modificaiton. Examination of m6A sites in murine brain RNA and human embryonic kidney cells.
2012-12-31 | E-GEOD-34734 | biostudies-arrayexpress
Project description:Here, we use a novel technique for locating regions of N6-adenosine methylation (m6A) throughout the transcriptome and present a profile of m6A sites in the mouse brain. Our use of methylated RNA immunoprecipitation combined with RNA-seq (MeRIP-Seq) identifies thousands of RNAs which contain m6A sites. In addition, we find that regions of m6A formation are particularly enriched near stop codons, which might provide clues into the potential funciton of this highly prevalent RNA modificaiton.
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Project description:Methylation of the N(6) position of adenosine (m(6)A) is a posttranscriptional modification of RNA with poorly understood prevalence and physiological relevance. The recent discovery that FTO, an obesity risk gene, encodes an m(6)A demethylase implicates m(6)A as an important regulator of physiological processes. Here, we present a method for transcriptome-wide m(6)A localization, which combines m(6)A-specific methylated RNA immunoprecipitation with next-generation sequencing (MeRIP-Seq). We use this method to identify mRNAs of 7,676 mammalian genes that contain m(6)A, indicating that m(6)A is a common base modification of mRNA. The m(6)A modification exhibits tissue-specific regulation and is markedly increased throughout brain development. We find that m(6)A sites are enriched near stop codons and in 3' UTRs, and we uncover an association between m(6)A residues and microRNA-binding sites within 3' UTRs. These findings provide a resource for identifying transcripts that are substrates for adenosine methylation and reveal insights into the epigenetic regulation of the mammalian transcriptome.
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Project description:The genetic code that specifies the identity of amino acids incorporated into proteins during protein synthesis is almost universally conserved. Mitochondrial translation deviates from the standard genetic code which includes the reassignment of two arginine codons into stop codons {Jukes, 1993 #438}. Translation termination at these non-canonical stop codons requires a protein factor to release the newly synthesized polypeptide chain, however, the identity of this factor is not known currently{Nadler, 2021 #406}. Here, we used gene editing and ribo-profiling in combination with cryo-electron microscopy to establish that the unusual mitochondrial release factor 1 (mtRF1) detects the non-canonical stop codons. We show that loss of mtRF1 leads to stalling of mitochondrial ribosomes on non-canonical stop codons and consequent reduced translation of cytochrome C oxidase subunit 1 that results in decreased mitochondrial respiration. We show that binding of mtRF1 to the decoding center of the ribosome stabilizes a highly unusual distortion in the mRNA conformation and that the ribosomal RNA importantly participates in the specific recognition of the non-canonical stop codons.
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Project description:In eukaryotes, the intrinsic mRNA stability is generally dictated by codon usage bias, the uneven preferences for synonymous codons, in a translation-dependent manner. However, the conserved mechanism underlining this phenomenon remains elusive. Hidden stop codons (HSCs), which are stop codons located in the +1 or -1 frame relative to canonical open reading frames (ORF), are sidespread across all genomes but have long been overlooked. We demonstrate that in both fungi and mammals, HSCs play an important role in regulating mRNA decay across the genome by immediately terminating out-of-frame translations promoted by nonoptimal codons, primarily through +1 ribosomal frameshifting. In the filamentous fungus Neurospora, partially deleting HSCs via synonymous substitutions in the clock gene frequency disrupts the circadian rhythm due to increased mRNA stability. Similarly, in human cells, impaired translation termination caused by rapid depletion of eRF1 leads to globally increased stability of mRNAs enriched with non-optimal codons and HSCs, which are in part degraded through the NMD pathway via UPF1. Given that from yeasts to humans the occurrence of HSCs is genome-widely associated with the presence of nonoptimal codons, these findings suggest that in eukaryotes, HSCs might coevolve with codon usage to modulate mRNA stabilities via immediately terminating different levels of ribosomal frameshifting events promoted by nonoptimal codons.
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Project description:The conserved and essential DEAD-box RNA helicase Ded1p from yeast and its mammalian ortholog DDX3 are critical for translation initiation. Mutations in DDX3 are linked to tumorigenesis and intellectual disability, and the enzyme is targeted by diverse viruses. How Ded1p and its orthologs engage RNAs to impact translation initiation has been a longstanding, unresolved question. Here we show that Ded1p associates with the pre-initiation complex at the mRNA entry channel of the small ribosomal subunit and that the helicase unwinds mRNA structure ahead of the scanning pre-initiation complex. Defective Ded1p causes pervasive translation in 5’UTRs, starting from near-cognate initiation codons located 5' of mRNA structures and concomitant decrease of protein synthesis from of the main ORFs. The data indicate that Ded1p functions to suppress translation initiation on near-cognate codons proximal to mRNA structure and show how the helicase is targeted to specific RNA sites without common sequence signatures. Our results reveal a straightforward mechanism for the activation of upstream open reading frames and suggest that mRNA structure and proximal near-cognate initiation codons encode a widespread regulatory program for translation initiation that is sensitive to RNA helicase function.
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Project description:mtRF1 recognises non-canonical stop codons in human mitochondria
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Project description:Stop codon readthrough (SCR) has important biological implications but remains largely uncharacterized. Here, we identify 1,009 SCR events in plants using a proteogenomic strategy. Plant SCR candidates tend to have shorter transcript lengths and fewer exons and splice variants than non-SCR transcripts. Mass spectrometry evidence shows that stop codons involved in SCR events can be recoded as 20 standard amino acids, some of which are also supported by suppressor transfer RNA analysis. We also observe multiple functional signals in 34 maize extended proteins and characterize the structural and subcellular localization changes in the extended protein of BASIC TRANSCRIPTION FACTOR 3. Furthermore, the SCR events exhibit non-conserved signature and the extensions likely undergo protein-coding selection. Overall, our study not only characterizes that SCR events are commonly present in plants but also identifies the unprecedented recoding plasticity of stop codons, which provides important insights into the flexibility of genetic decoding.
2024-02-02 | PXD038762 | Pride
Project description:Stop codon readthrough (SCR) has important biological implications but remains largely uncharacterized. Here, we identify 1,009 SCR events in plants using a proteogenomic strategy. Plant SCR candidates tend to have shorter transcript lengths and fewer exons and splice variants than non-SCR transcripts. Mass spectrometry evidence shows that stop codons involved in SCR events can be recoded as 20 standard amino acids, some of which are also supported by suppressor transfer RNA analysis. We also observe multiple functional signals in 34 maize extended proteins and characterize the structural and subcellular localization changes in the extended protein of BASIC TRANSCRIPTION FACTOR 3. Furthermore, the SCR events exhibit non-conserved signature and the extensions likely undergo protein-coding selection. Overall, our study not only characterizes that SCR events are commonly present in plants but also identifies the unprecedented recoding plasticity of stop codons, which provides important insights into the flexibility of genetic decoding.
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Project description:Mitochondrial translation system highly diverged from its bacterial counterpart. This includes deviation from the universal genetic code, with AGA and AGG having no cognate tRNAs in human mitochondria. Their locations at the end of COX1 and ND6 open reading frames, respectively, suggests they function as stop codons. However, while canonical stop codons, UAA and UAG, are recognized by mtRF1a in mitochondria, the release mechanism at AGA and AGG remains a debated issue. Here, we show that upon the loss of another member of the mitochondrial release factor family, mtRF1, mitoribosomes accumulate specifically at AGA and AGG codons. Stalling of mitoribosomes alters COX1 transcript and protein levels, but not ND6 production. Finally, we set up an in vitro reconstituted mitochondrial translation system, which confirms the specific release activity of mtRF1 on AGA and AGG codons. Together, our study uncovers the mechanism of translation termination in mitochondria and provides first insights into the consequences of its failure.
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